Affiliation:
1. Department of Dermatology, Boston University School of Medicine, 609 Albany Street Boston, MA, 02118, United States
2. Division
of Pharmaceutical Sciences, James L. Winkle College of Pharmacy, University of Cincinnati, Cincinnati, OH, 45229, United States
Abstract
Abstract:
Monkeypox is a zoonotic viral disease and remains endemic in tropical regions of Central and West Africa.
Since May of 2022, cases of monkeypox have soared and spread worldwide. Confirmed cases have shown no
travel history to the endemic regions as seen in the past. The World Health Organization declared monkeypox a
global public health emergency in July 2022, and the United States government followed suit one month later. The
current outbreak, in contrast to traditional epidemics, has high coinfection rates, particularly with HIV (human immunodeficiency
virus), and to a lesser extent with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2),
the pathogen of COVID-19. No drugs have been approved specifically for monkeypox. However, there are therapeutic
agents authorized to treat monkeypox under the Investigational New Drug protocol, including brincidofovir,
cidofovir, and tecovirimat. In contrast to limited options for monkeypox treatment, there are available drugs specifically
for HIV or SARS-CoV-2 infection. Interestingly, these HIV and COVID-19 medicines share metabolism pathways
with those authorized to treat monkeypox, particularly of hydrolysis, phosphorylation, and active membrane
transport. This review discusses how these pathways shared by these medicines should be considered to gain therapeutic
synergy and maximize safety for treating monkeypox coinfections.
Funder
National Institutes of Health
Publisher
Bentham Science Publishers Ltd.
Subject
Clinical Biochemistry,Pharmacology